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An immunosuppressant, FK506, protects hippocampal neurons from forebrain ischemia in the mongolian gerbil.

作者信息

Ide T, Morikawa E, Kirino T

机构信息

Department of Neurosurgery, Faculty of Medicine, University of Tokyo, Japan.

出版信息

Neurosci Lett. 1996 Feb 9;204(3):157-60. doi: 10.1016/0304-3940(96)12352-1.

DOI:10.1016/0304-3940(96)12352-1
PMID:8938254
Abstract

We examined whether an immunosuppressant, FK506, inhibits delayed neuronal death in the gerbil hippocampal CA1 sector after 5-min forebrain ischemia. After reperfusion, gerbils were injected intravenously with FK506. Gerbils in the early injection group were injected with FK506 immediately after reperfusion, and gerbils in the delayed injection group were injected with FK506 1 or 2 h postischemia. The body temperature of the FK506-treated gerbils in the normothermic group was maintained at 37.5-38.0 degrees C for 2 h postischemia. In the chronic survival group, neuroprotection was assessed after recovery for 45 days. Seven or 45 days after reperfusion, neuronal density in the CA1 was assessed following perfusion fixation. FK506 ameliorated cell death in the CA1 in a dose-dependent manner in every group, although it showed a hypothermic effect. FK506 is neuroprotective against forebrain ischemia in gerbils.

摘要

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1
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引用本文的文献

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Stroke Res Treat. 2012;2012:809417. doi: 10.1155/2012/809417. Epub 2011 Sep 15.
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Calcineurin-mediated BAD dephosphorylation activates the caspase-3 apoptotic cascade in traumatic spinal cord injury.
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Cyclosporin A, but not FK 506, protects mitochondria and neurons against hypoglycemic damage and implicates the mitochondrial permeability transition in cell death.环孢素A而非FK506可保护线粒体和神经元免受低血糖损伤,并表明线粒体通透性转换与细胞死亡有关。
J Neurosci. 1998 Jul 15;18(14):5151-9. doi: 10.1523/JNEUROSCI.18-14-05151.1998.
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